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The JC polyomavirus (JCV) VP1 capsid protein-derived peptides presented by patient HLA class I molecules are the primary targets for the cellular immune response against JCV infection (Koralnik et al., 2002) [1]. JCV is a double-stranded DNA virus that causes Progressive Multifocal Leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system, primarily in immunocompromised individuals (Lima et al., 2010) [2]. The VP1 protein is the major capsid protein of the virus and contains specific peptide sequences, such as the immunodominant VP1 100-108 epitope, which are processed and displayed by HLA class I molecules (e.g., HLA-A*02:01) on the surface of infected cells (Jelcic et al., 2013) [3]. Recognition of these peptide-MHC complexes by CD8+ cytotoxic T lymphocytes (CTLs) is essential for controlling viral replication and preventing the progression of PML. Therapeutic interventions currently under investigation include the adoptive transfer of JCV-specific or cross-reactive BK virus-specific T cells to restore the immune system's ability to target these VP1-HLA complexes (Muftuoglu et al., 2018) [4]. Additionally, these complexes serve as critical biomarkers for monitoring the restoration of anti-viral immunity and predicting patient survival in clinical settings.
Recognition by cytotoxic CD8+ T lymphocytes (CTLs) leading to the targeted lysis of JCV-infected cells in the central nervous system.
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